尽管雷公藤多苷（GTW）已广泛用于治疗慢性肾脏病（CKD），但其药理学机制有待研究阐明。盐敏感性高血压是导致CKD的主要病因之一。我们发现GTW抑制盐敏感性高血压所致的肾脏损害，但机制不清。新近研究证实单核/巨噬细胞促进盐敏感性高血压等多种疾病所致的CKD。为此，我们将利用特异性的单核/巨噬细胞清除药（liposome-clodronate）在盐敏感性高血压动物模型上，明确GTW对单核/巨噬细胞功能的影响作用，以及该作用对肾脏损害的影响。另外，通过单核/巨噬细胞培养模型，探明在炎性因素刺激下GTW中最主要的活性物质雷公藤甲素对单核/巨噬细胞的功能表型（M1和M2）及其信号转导通路的影响。因此，本研究将阐明GTW调节单核/巨噬细胞功能的分子生物学机制，从而揭示GTW抑制盐敏感性高血压所致肾脏损害的药理学机制，并为该药用于治疗CKD提供坚实的药理学实验基础。

Although multi-glycoside of Tripterygium wilfordii Hook F (GTW) is used widely for the treatment of chronic kidney disease (CKD), the pharmacological mechanisms are not fully elucidated. Salt-sensitive hypertension is one of major causes leading to CKD. We found that GTW attenuated renal injury in salt-sensitive hypertension, but the mechanisms are not determined. Recent studies have shown that monocyte/macrophage aggravates CKD induced by several diseases including salt-sensitive hypertension. Thus we will determine the effects of GTW on monocyte/macrophage, and its effects on renal injury using a manipulation for selective depletion of macrophages (liposome-clodronate) in salt-sensitive hypertension. Furthermore, using an in vitro culture model of monocyte/ macrophage, we will clarify the actions of triptolide, a primary active compound derived from GTW, on macrophage polarization (M1 and M2) and its signaling pathway under stimulation of inflammation. So our data will elucidate the molecular mechanisms responsible for GTW-mediated modulation of monocyte/macrophage, which may constitute the pharmacological mechanisms by which GTW attenuates renal injury in salt-sensitive hypertension. More importantly, our work will provide the solid pharmacological evidence for the use of GTW in the treatment of CKD.